While gender differences in human myocardial responses to stress have been observed, the cellular events mediating these differences are unknown. Myocardial contractile responses to stress are primarily mediated by beta-adrenergic receptor stimulation. Beta-adrenergic receptor activation results in a greater Ca2+ influx (Ca2+ current) through membrane L-type Ca2+ channels. The specific aims of this proposed study are: 1) to determine sex differences in number and properties of L-type Ca2+ channels and 2) to determine sex differences in the basal and isoproterenol-stimulated Ca2+ current. Specific aim 1 will be addressed using protein (Ca2+ channel) binding studies in male and female rat atrial and ventricular membranes. Specific aim 2 will be addressed using whole-cell current recording studies in isolated atrial and ventricular myocytes from male and female rats. The long-term objective of this plan of research is to identify and understand the electrophysiologic basis of human gender differences in beta-adrenergic mediated effects on myocardial contractility. Elucidating electrophysiologic mechanisms mediating these gender differences establishes a physiologic basis for nursing practice in evaluating and treating stress-associated myocardial dysfunctions.